Using the electron microscope and techniques such as negative staining, thin sectioning and ferritin-labelling of specific antibody to individual components, we plan to continue our studies on the topographical relationship between key complement components and ultrastructural lesions on cell membranes. Comparisons will be made between membranes on which complement has been activated by the classic mechanism with those on which complement was activated by the alternate mechanisms. Since activation of complement by both mechanisms leads to the production of ultrastuctural lesions but only activation by the classic mechanism leads to cytolysis, it is hoped that these studies will lead to a better understanding of the mechanism of cell lysis. We plan to continue our studies of the complement receptors on lymphocytes in both normal individuals and in certain disease states, our ultimate goal being to determine the role of lymphocyte complement receptors in the immune response. We will also pursue further our studies with complement receptors on other cell types and determine the role of these receptors in important biologic phenomenon such as phagocytosis. We plan to continue and expand our studies on the role of complement in cystic fibrosis. We will determine the relationship between the basic peptide associated with the complement system and the cystic fibrosis factors. We plan to determine whether the aberrations in activity of certain of the complement components are of primary or secondary origin in this disease state. BIBLIOGRAPHIC REFERENCES: Ross, G.D. and Polley, M.J. Specificity of Human Lymphocyte complement receptors. J. Exp. Med. 141, 1163, 1975. Polley, M.J. and Nachman, R.L. Ultrastructural lesions on the surface of platelets associated with either blood coagulation or with antibody-mediated immune injury. J. Exp. Med. 141, 1261, 1975.